Model Status

This CellML runs in both OpenCell and COR but there are several unit inconsistencies. Further curation is required to get the model to run to recreate the published results.

Model Structure

ABSTRACT: Dogs have been used extensively to study atrial arrhythmias, but there are no published mathematical models of the canine atrial action potential (AP). To obtain insights into the ionic mechanisms governing canine atrial AP properties, we incorporated formulations of K(+), Na(+), Ca(2+), and Cl(-) currents, based on measurements in canine atrial myocytes, into a mathematical model of the AP. The rate-dependent behavior of model APs corresponded to experimental measurements and pointed to a central role for L-type Ca(2+) current inactivation in rate adaptation. Incorporating previously described regional ionic current variations into the model largely reproduced AP forms characteristic of the corresponding right atrial regions (appendage, pectinate muscle, crista terminalis, and atrioventricular ring). When ionic alterations induced by tachycardia-dependent remodeling were incorporated, the model reproduced qualitatively the AP features constituting the cellular substrate for atrial fibrillation. We conclude that this ionic model of the canine atrial AP agrees well with experimental measurements and gives potential insights into mechanisms underlying functionally important electrophysiological phenomena in canine atrium.

A schematic representation of the canine atrial myocyte. Intracellular compartments indicate the intracellular pools of ion species. The ion concentration in each pool is affected by ionic currents, pumps and exchangers. The sarcoplasmic reticulum is divided into two compartments: the Ca2+ release compartment, or junctional sarcoplasmic reticulum (JSR) and the Ca2+ uptake compartment, or network sarcoplasmic reticulum (NSR).